In 1950, medical physicist John Gofman, University of California, published an article in Science pointing out that, as a guide, total cholesterol was “false and highly dangerous” – a poor predictor of heart disease risk.

Using a one-of-a-kind ultra-centrifuge, Gofman identified the various lipoproteins and concluded that fat (triglycerides) carried in the blood by VLDL – not cholesterol – was the reliable predictor of heart disease.

It was carbohydrates, Gofman reported, that elevated VLDL. Only by restricting carbohydrates could VLDL be lowered. According to Gofman, total cholesterol measurements tell us nothing about the status of VLDL and LDL.

Prescribing low fat, high carb diets, he said, would increase heart disease risk for a large percentage of the population. “Neglect of the carbohydrate factor can lead to rather serious consequences,” Gofman wrote in 1958.

According to Gary Taubes in Good Calories, Bad Calories, as early as 1955, Pete Ahrens at Rockefeller University had come to the same conclusion as Gofman. Ahrens had reported that triglycerides shoot up on a low fat diet – and fall on a high fat diet:

“The percent of fat in the blood rises with the severity of [heart] disease … and is especially related to the quantity of carbohydrate, which is being oxidized, rather than with the fat being administered.”

But measuring triglycerides was more difficult than measuring cholesterol, and the cholesterol bandwagon had already left the station. The National Institutes of Health had committed its resources to three expensive diet heart studies measuring only cholesterol – including funding for Ancel Key’s Seven Countries Study.

According to Gary Taubes, as the federal government sidled up to Ancel Keys’ “low fat equals good health” mantra, “No consideration was given to any alternative hypothesis.” Gofman subsequently lost interest in lipid research and a bevy of researchers, including Pete Ahrens at Rockefeller University, were simply ignored.

Comparing the different effects of dietary fat and dietary carbohydrate on lipids in our blood:

High Fat Breakfast – Two eggs fried in two tablespoons of butter

When you eat a fat- and protein-rich breakfast, the fat begins separating from the protein in the stomach and is absorbed as individual molecules inside the intestinal wall. Here the fatty acids are re-packaged into triglycerides (3 fatty acids attached to glycerol) and are loaded onto the mighty chylomicrons – 18-wheelers delivering dietary fat out to the body.

Chylomicrons travel until they have delivered their fatty bounty, shrink and disappear (remnants are picked up by the liver). Because chylomicrons have the specific apoB-48 protein attached, we know that hungry cells quickly snatch up this fat – of dietary origin.

For 2 or 3 hours after our high fat breakfast, we will see elevated chylomicron levels that fall quickly. Chylomicrons – apoB48s – are too small and too few to be measured in blood work and they have no direct effect on liver-made VLDL or LDL.

High Carbohydrate Breakfast – Cup of Cheerio’s, cup of skim milk, washed down with some orange juice

After our high carb breakfast, there is no immediate effect on lipid levels; instead you get an immediate rise in blood sugar and insulin. (The very first bite of Cheerios will send a pulse of insulin into the blood.) Starches and sugars (glucose) are soluble in water so they are readily absorbed into the blood (except fructose which is sent to the liver via the portal vein).

In short order, the high carb breakfast creates a metabolic traffic jam in the liver. The fructose arriving via the portal vein is being converted into fat, and – at the direction of insulin – excess glucose arriving in the blood also must be converted into fat – a triglyceride double whammy!

VLDL production will continue for several hours (8 to 10) after a carb-loaded breakfast. Chronic excess carb intake will trigger elevated triglycerides requiring ever-new fleets of VLDL to haul away the fat – exactly what Gofman and Ahrens (and Dr. Atkins) warned us about.

Fifty years ago, Peter Ahrens called excess fat in the blood: Carbohydrate-induced lipemia. Today, doctors are grappling with the same set of symptoms, now referred to as Metabolic Syndrome, affecting 25 percent of the population, including – for the first time – plenty of teenage children:

Elevated Triglycerides (TG)

Elevated VLDL

depressed HDL reverse transport

sharp increase in number of small, dense oxidized LDL particles

increased risk of heart disease.

The history of the Diet Heart hypothesis is riddled with scientific missteps and even outright fraud. If you agree that low fat has failed the test of time, please pass this article on. Thank you!

Spot on. I’m a retired doctor with a career-long interest in heart disease, though not my speciality at all.
All of this stuff is apparent to those with an open mind. This kind of thing explains ALL the Paradoxes, like the French Paradox, the Roseto Italians etc etc. It’s obviously right.
Unfortunately this can only be seen by somone looking at the evidence from scratch, or someone like myself who is very open-minded, even though I say so myself.
For the biggest clinical trial ever, I give you the people of France.

Excellent site you have here but I was wondering if you knew of
any discussion boards that cover the same topics discussed in this article?
I’d really love to be a part of community where
I can get feedback from other knowledgeable individuals that share the
same interest. If you have any recommendations, please let me know.
Thanks a lot!